Alzheimer's disease (AD) is a disease in which the degeneration of nerve cells in the brain is thought to lead to dementia. The most plausible hypothesis for the pathogenic mechanism of Alzheimer's disease is “amyloid hypothesis”, which proposes that the accumulation of β-amyloid (hereinafter, sometimes abbreviated as “Aβ”) in the brain is the beginning of the disease. It is considered that soluble Aβ strongly inhibits long-term potentiation of memory, and deposits of aggregated Aβ form fibril, thereby leading to neuronal cell death.
Non-patent document 1 discloses that administration of anti-Aβ antibodies, that is an antibody against Aβ, and Aβ vaccines leads to not only improvement in the symptoms of dementia but also disappearance of Aβ deposition in the brain, suggesting the possibility of cure for Alzheimer's disease.
However, while the development of anti-Aβ antibodies with excellent therapeutic effect has been advanced by a large number of research groups, treatment with the anti-Aβ antibody places a great burden on patients since it is expensive and takes long time. Also, there is another problem that owing to a relatively short efficacy of anti-Aβ antibody treatment, repetitive administration becomes necessary.
Further, as evidenced by such an incident that a clinical trial was discontinued due to death caused by an adverse reaction of Aβ vaccine administration (Non-patent document 2), there is still a long way to the establishment of therapy for Alzheimer's disease.
Experiments using mouse models of Alzheimer's disease show that the amount of Aβ in blood significantly increases as the brain Aβ decreases (Non-patent document 3), peripheral administration of non-immunostimulatory Aβ-binding substances (i.e., gelsolin and GM1 ganglioside) reduces the amount of Aβ in the brain (Non-patent documents 4 and 5), administration of non-immunostimulatory anti-Aβ antibody Fab fragments via the blood reduces the amount of Aβ in the brain (Non-patent document 6), and so on, from which the “sink hypothesis”, meaning that the efflux of Aβ from the brain into the blood occurs as the amount of Aβ in blood decreases, is proposed. Also, in relation with this hypothesis, Non-patent documents 7 and 8 disclose that the amount of Aβ in blood is reduced by artificial dialysis.
Further, patent documents 1-3 disclose technology relating to an Aβ remover, which removes Aβ in blood by extracorporeal circulation of the blood.